19542-67-7

Basic information

• Product Name: BAY 11-7082
• Synonyms: BAY 11-7082;BAY 11-7821;(E)-3-(4-METHYLPHENYLSULFONYL)-2-PROPENENITRILE;(2E)-3-[(4-METHYLPHENYL)SULFONYL]-2-PROPENENITRILE;(E)-3-tosylacrylonitrile;(E)-3-(p-Toluenesulfonyl)acrylonitrile;BAY11-7082/BAY117082;BAY11-7082,BAY 117821
• CAS NO: 19542-67-7
• Molecular Formula: C₁₀H₉NO₂S
• Molecular Weight: 207.25
• Product Categories: Cytokine signaling;NF-kB;Inhibitors
• Mol File: 19542-67-7.mol
• Article Data: 12

Chemical Properties

• Melting Point: 133-135℃
• Boiling Point: 397.6°Cat760mmHg
• Flash Point: 194.3°C
• Appearance: white/solid
• Density: 1.237g/cm³
• Vapor Pressure: 1.57E-06mmHg at 25°C
• Refractive Index: 1.557
• Storage Temp.: Store at +4°C
• Solubility: DMSO: 25 mg/mL, soluble
• Stability: Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 3 months.
• CAS DataBase Reference: BAY 11-7082(CAS DataBase Reference)
• NIST Chemistry Reference: BAY 11-7082(19542-67-7)
• EPA Substance Registry System: BAY 11-7082(19542-67-7)

Safety Data

• WGK Germany: 3
• RTECS: UD1430000
• Hazardous Substances Data: 19542-67-7(Hazardous Substances Data)

Usage

Description

BAY 11-7082 (19542-67-7)?inhibits cytokine-induced IκB-α phosphorylation via inhibition of IκB Kinase which results in inhibition of NFκB .1 Inhibits anchorage-independent growth of mammary epithelial cells induced with 4-hydroxyestradiol via inhibition of NFκB activation.2 Inhibits IFNα production and blocks nuclear translocation of IRF7 in plasmacytoid dendritic cells.3? Facilitates wound healing by inhibiting TNFα-induced MMP expression.4 A useful tool for probing the involvement of NFκB in physiological and pathophysiological processes.5? Cell permeable.

Uses

Bay 11-7082 has been used as:a nuclear factor-kappa B (NF-kB) inhibitor to verify the action of the NF-kB signaling pathway in the production of interleukin (IL)-8a nuclear factor-kappa B (NF-kB) inhibitor to study the role of NF-kB activation in Mycoplasma hyorhinis -induced epithelial-mesenchymal transition (EMT) and cell migrationa nod-like receptor family pyrin domain containing 3 (NLRP3) selective inhibitor to examine its effects on liver inflammation in mice after hematopoietic stem cell transplantation

Definition

ChEBI: A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation i cells.

General Description

Potential anti-inflammatory agent that selectively and irreversibly inhibits the TNF-α-inducible phosphorylation of IκBα (IC50 = 10 μM), resulting in a decreased expression of NF-κB and of adhesion molecules. Does not affect constitutive IκBα autophosphorylation. Inhibits TNF-α-induced surface expression of the endothelial-leukocyte cell adhesion molecules E-selectin, VCAM-1, and ICAM-1. A 100 mM (10 mg/483 μl) solution of BAY 11-7082 (Cat. No. 196871) in DMSO is also available is also available.

Biological Activity

Irreversible inhibitor of TNF- α -stimulated I κ B α phosphorylation (IC 50 ~ 10 μ M); leads to decreased NF- κ B and subsequent decreased expression of adhesion molecules. Also reversibly activates MAP kinases and stimulates apoptosis.

Biochem/physiol Actions

Bay 11-7082 acts as a selective inhibitor for nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway. In addition, to the inhibition of nuclear factor-kappa B (NF-kB), Bay 11-7082 also triggers apoptosis in anucleated erythrocytes, human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines and primary adult T-cell leukemia cells.

Enzyme inhibitor

This protein kinase inhibitor (FW = 207.31 g/mol; CAS 19542-67-7; lmax = 251 nm), also named 3-[(4-methylphenyl)sulfonyl]-(2E)-propenenitrile, targets NF-κB activation, selectively and irreversibly blocking TNF-α- induced phosphorylation of IκB-α without affecting phosphorylation of constitutive IκB-α. Mechanism of Inhibitory Action: NF-κB transcription factor regulates expression of inflammatory cytokines, various chemokines and immunoreceptors, as well as cell adhesion molecules. When stationed within the cytoplasm, NF-κB is kept inactive through its binding to the inhibitory factor IκB; however, certain stimuli result in IκB phosphorylation and ubiquitin-mediated degradation, freeing NF-κB for translocation to the nucleus. In endothelial cells, IκB-α phosphorylation and degradation occur within 15 min of TNFα treatment, allowing NF-κB to translocate to the nucleus to activate gene expression. Treatment of humnan vascular endothelial cells (HUVEC) with TNFα results in rapid loss of IκB-α from the cytoplasm. BAY11-7082 stabilizes IκB-α in a dose-dependent manner (IC50 ≈ 10 μM). There is a clear correlation between the concentration of drug that stabilizes IκB-α, the concentration that inhibits nuclear levels of NF-κB, and the concentration that inhibits adhesion molecule expression. More recent studies demonstrate that BAY 11- 7082 prevents ubiquitin conjugation to Ubc13 and UbcH7 by forming a covalent adduct with their cysteine residues via Michael addition at the C-3 atom of BAY 11-7082, followed by the release of 4-methylbenzenesulfinate. BAY 11-7082 stimulated Lys48-linked polyubiquitin chain formation in cells and protected Hypoxia-Inducible Factor-1α (HIF1α) from proteasomal degradation, suggesting it inhibits the proteasome. These results indicate that the anti-inflammatory effects of BAY 11-7082, its ability to induce B-cell lymphoma and leukemic T-cell death and to prevent the recruitment of proteins to sites of DNA damage are exerted via inhibition of components of the ubiquitin system– not by inhibiting NF-κB. BAY11-7082 also inhibits proliferation and promotes apoptosis in breast carcinoma MCF-7 cells by inhibiting phosphorylation of ATP citrate lyase.

References

1) Pierce et al. (1997) Novel inhibitor of cytokine-induced IkBα phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo; J. Biol. Chem., 272 21096 2) Park et al. (2009) 4-hydroxyestradiol induces anchorage-independent growth of human mammary epithelial cells via activation of IkappaB kinase: potential role of reactive oxygen species; Cancer Res., 69 2416 3) Miyamoto et al. (2010) Inhibitor of IkappaB kinase activity, BAY 11-7082, interferes with interferon regulatory factor 7 nuclear translocation and type I interferon production by plasmacytoid dendritic cells; Arthritis Res. Ther., 12 R87 4) Xu et al. (2019) Bay 11-7082 facilitates wound healing by antagonizing mechanical injury – and TNF-α-induced expression of MMPs in posterior cruciate ligament; Connect. Tissue Res. 60 311 5) Kim et al. (2018) TNF-α induces human neural progenitor cell survival after oxygen-glucose deprivation by activating the NFκB pathway; Exp. Mol. Med., 50 14

InChI:InChI=1/C10H9NO2S/c1-9-3-5-10(6-4-9)14(12,13)8-2-7-11/h2-6,8H,1H3/b8-2+

Upstream product

• 871-29-4 trans-β-chloroacrylonitrile 
• 824-79-3 sodium 4-methylbenzenesulfinate 
• 151-50-8 potassium cyanide 
• 86409-95-2 (E)-1-(phenylseleno)-2-(p-tolylsulfonyl)ethene Se-oxide 
• 107-13-1 acrylonitrile 
• 1576-35-8 toluene-4-sulfonic acid hydrazide 
• 13894-21-8 ethynyl p-tolyl sulfone 
• 75-86-5 2-hydroxy-2-methylpropanenitrile 
• 98-59-9 p-toluenesulfonyl chloride 
• 1950-78-3 p-toluenesulfonyl iodide 
• 68819-94-3 p-tolyl benzeneselenosulfonate 
• 86409-89-4 (E)-1-(phenylseleno)-2-(p-tolylsulfonyl)ethene 
• 7569-26-8 chloromethyl p-tolylsulfone 
• 107-14-2 chloroacetonitrile 

Downstream Products

• 1950-69-2 toluene-p-sulfonyl bromide 
• 14028-37-6 α,β-Dibrom-β-(p-tolylsulfonyl)-propionitril 
• 715-12-8 (E)-3-(p-toluenesulfonyl)-acrylic acid 
• 24237-80-7 3-morpholin-4-yl-3-(toluene-4-sulfonyl)-propionitrile 

Related news

Research paperSuppression of NF-κB and NF-κB regulated oxidative stress and neuroinflammation by BAY 11-7082 (cas 19542-67-7) (IκB phosphorylation inhibitor) in experimental diabetic neuropathy08/28/2019

Inflammation is an emerging patho-mechanism of diabetes and its complications. NF-κB pathway is one of the central machinery initiating and propagating inflammatory responses. The present study envisaged the involvement of NF-κB inflammatory cascade in the pathophysiology of diabetic neuropath...detailed

Inhibition of NF-κB activity by BAY 11-7082 (cas 19542-67-7) increases apoptosis in multidrug resistant leukemic T-cell lines08/27/2019

Multidrug resistance (MDR) is the main reason for failure of cancer therapy with resistance to apoptosis being one of the mechanisms involved. Constitutive NF-κB activity has been detected in many tumors contributing to oncogenesis and tumor survival whereas inhibition of NF-κB activity has pr...detailed

The inhibitor of IkappaBalpha phosphorylation BAY 11-7082 (cas 19542-67-7) prevents NMDA neurotoxicity in mouse hippocampal slices08/26/2019

NF-κB is a nuclear transcription factor involved in the control of fundamental cellular functions including cell survival. Among the many target genes of this factor, both pro- and anti-apoptotic genes have been described. To evaluate the contribution of NF-κB activation to excitotoxic insult,...detailed

BAY 11-7082 (cas 19542-67-7) induces cell death through NF-κB-independent mechanisms in the Ewing’s sarcoma family of tumours08/25/2019

The role of NF-κB in the Ewing’s sarcoma family of tumours (ESFT) and their response to fenretinide has been investigated. Basal levels of phosphorylated NF-κB were low in all ESFT cells. BAY 11-7082 decreased cell viability, which was accompanied by caspase-3 cleavage. This was independent o...detailed

BAY 11-7082 (cas 19542-67-7) ameliorates diabetic nephropathy by attenuating hyperglycemia-mediated oxidative stress and renal inflammation via NF-κB pathway08/23/2019

Diabetic nephropathy is a serious microvascular complication for patients associated with diabetes mellitus. Recent studies have suggested that NF-κB is the main transcription factor for the inflammatory response mediated progression of diabetic nephropathy. Hence, the present study is hypothes...detailed

In Vivo Short-Term Topical Application of BAY 11-7082 (cas 19542-67-7) Prevents the Acidic Bile–Induced mRNA and miRNA Oncogenic Phenotypes in Exposed Murine Hypopharyngeal Mucosa1208/22/2019

PURPOSE: Bile-containing gastroesophageal reflux may promote cancer at extraesophageal sites. Acidic bile can accelerate NF-κB activation and molecular events, linked to premalignant changes in murine hypopharyngeal mucosa (HM). We hypothesize that short-term in vivo topical application of NF-κ...detailed

Relevant articles and documents

PROCESS FOR THE PREPARATION OF ARYLSULFONYLPROPENENITRILES

The present invention relates to a process for the preparation of arylsulfonylpro- penenitriles. The reaction starting from arylsulfonyl halides is catalyzed by a cat- alyst compound comprising a transition metal. The process is scalable, environ- mentally benign and provides the product in good yield.

PROCESS FOR THE PREPARATION OF ARYLSULFONYLPROPENENITRILES BY PHOTOCATALYTIC REACTIONS

The present invention relates to a process for the preparation of arylsulfonylpro- penenitriles. The reaction starting from arylsulfonyl iodides is catalyzed by light. The process is scalable, environmentally benign and provides the product in good yield.

An improved synthesis of vinyl- and β-iodovinyl sulfones by a molecular iodine-mediated one-pot iodosulfonationdehydroiodination reaction

An improved one-pot method to synthesize vinyl sulfones from unsaturated systems by using molecular iodine/sodium arenesulfinate/sodium acetate as reagents was described. Vinyl sulfones derived from styrene derivatives were generally obtained in good to excellent yields except for those bearing strong electron releasing substituent. Aliphatic alkenes and activated alkenes gave the corresponding vinyl sulfone products in moderate to good yields. Arylacetylenes yielded the respective β-iodovinyl sulfones in good yields while low yield was observed with aliphatic terminal alkyne. The potentials of the method entail simplicity, short reaction time, non-anhydrous reaction conditions, employing inexpensive, non-metallic reagent and integrating two reactions that are commonly accomplished separately into a single operation. Supplemental materials are available for this article. Go to the publisher's online edition of Synthetic Communications to view the free supplemental file. Copyright Taylor & Francis Group, LLC.